Placental development in a mouse model of spinal muscular atrophy

Abstract

Spinal Muscular Atrophy (SMA) is an autosomal recessive disorder, leading to fatal loss of motor neurons. It is caused by loss of function of the SMN gene, which is expressed throughout the body, and there is increasing evidence of dysfunction in non-neuronal tissues. Birthweight is one of most powerful prognostic factors for infants born with SMA, and intrauterine growth restriction is common. In the SMNΔ7 mouse model of SMA, pups with the disease lived 25% longer when their mothers were fed a higher fat, “breeder” diet. The placenta is responsible for transport of nutrients from mother to fetus, and is a major determinant of fetal growth. Thus, the present study tested the hypothesis that placental development is impaired in SMNΔ7 conceptuses. Detailed morphological characterization revealed no defects in SMNΔ7 placental development, and expression of key transcription factors regulating mouse placental development was unaffected. The intrauterine growth restriction observed in SMA infants likely does not result from impaired placental development.

Deletion of fetoplacental Fshr inhibits fetal vessel angiogenesis in the mouse placenta

“…One utilizes vascular corrosion casts of placental fetal vessels that are scanned by x-ray microcomputed tomography and quantified (Rennie et al, 2015). The other method utilizes a quantitative morphometric approach in which maternal vs. fetal sinuses in the placental labyrinth are manually traced (identified by the presence vs. the absence of red blood cells, respectively), pseudo-colored, and quantified with Image J (Harper et al, 2015; Li et al, 2013; Schulz et al, 2012; Van Gronigen Caesar et al, 2016). We chose the latter method for this study because it afforded us the ability to quantitatively analyze potential changes in both the fetal and the maternal sinuses of the labyrinth.…”